Oncogenic role of the TP53-induced glycolysis and apoptosis regulator in nasopharyngeal carcinoma through NF-κB pathway modulation

Zhao,Ming; Fan,Juan; Liu,Yong; Yu,Yanxin; Xu,Jinhui; Wen,Qinglian; Zhang,Jianwen; Fu,Shaozhi; Wang,Biqiong; Xiang,Li; Feng,Jing; Wu,Jingbo; Yang,Linglin

doi:10.3892/ijo.2015.3297

Oncogenic role of the TP53-induced glycolysis and apoptosis regulator in nasopharyngeal carcinoma through NF-κB pathway modulation

Authors:
- Ming Zhao
- Juan Fan
- Yong Liu
- Yanxin Yu
- Jinhui Xu
- Qinglian Wen
- Jianwen Zhang
- Shaozhi Fu
- Biqiong Wang
- Li Xiang
- Jing Feng
- Jingbo Wu
- Linglin Yang
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Affiliations: Department of Oncology, The First Hospital of Sichuan Medical University, Luzhou, Sichuan 646000, P.R. China
Published online on: December 17, 2015 https://doi.org/10.3892/ijo.2015.3297
Pages: 756-764

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Abstract

The TP53-induced glycolysis and apoptosis regulator (TIGAR) is a p53 target gene, which functions to suppress reactive oxygen species (ROS) damage and protect cells from apoptosis. In this study, we investigated the role of TIGAR in nasopharyngeal carcinoma (NPC) tumorigenesis. Imnunohistochemical analysis of the tissue specimens from nasopharyngeal carcinoma patients showed a higher expression level of TIGAR in tumor tissues, compared with normal nasopharyngeal epithelium. Knockdown of TIGAR by lentivirus-shRNA in CNE-2 or 5-8F cells resulted in decreased cell growth, colony formation, migration, invasion, and induced apoptosis. TIGAR overexpression exerted the opposite effects except for apoptosis reduction. In the xenograft tumor models, TIGAR knockdown reduced tumor growth rate and weight, whereas TIGAR overexpression showed the opposite effects. In addition, the NF-κB signaling pathway was decreased in TIGAR silenced cells. In conclusion, our data demonstrated that TIGAR acted as an oncogene in NPC tumorigenesis, and knockdown of TIGAR inhibited NPC tumor growth through the NF-κB pathway.

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